Covariance between direct and maternal genetic effects on body weight in random-bred ICR mice at 2 through 10 weeks of age was estimated from cross-fostering experiments. The covariance contributes only a few percent of phenotypic variance at 2 weeks, but increases to 10–15% at later ages. Nearly all estimates are positive. We suggest that genes active during later parts of growth affect maternal performance more than those active during early growth, causing increased covariance at later ages. A model of combined genetic and persistent environmental effects on maternal performance is presented. Persistent effects of genetic or environmental variation in recent ancestors can influence covariance between relatives and response to selection.

We report the results of an ontogenetic analysis of quantitative genetic variance components with two replicates drawn from the randombred ICR strain of mice. A total of 432 mice from 108 full-sib families raised in a cross-fostering design were used to estimate direct effects heritability, maternal effects, and environmental effects for weight, head length, trunk length, trunk circumference, and tail length at 17, 24, 31, 38, 45, 52, 59, and 66 days of age. There was no significant difference in heritability between the replicates. Heritabilities either stayed more or less constant with age at about 0·30 (weight, trunk length, trunk circumference) or increased slightly with age (head length, tail length). Maternal effects decreased with age from a maximum of about 0·50 at weaning to about 0·15 at age 66 when growth was nearly complete. Environmental effects increased in relative importance during ontogeny.

Changes in brain size, body size and their co variance are reported from a long-term replicated directional selection experiment on body weight gain in rats. Two strains had been selected for increased and two for decreased weight gain between 3 and 9 weeks of age, and there were two randomly selected control lines. Selection produced significant changes in body weight in all selected lines. Divergence from the controls occurred in brain size in those strains selected for increased weight gain; no significant divergence was found for the strains selected for decreased weight gain. Divergence among unselected control lines suggests that genetic drift occurred in expression of brain size. Sexual dimorphism in response to selection results from sex differences in heritabilities and genetic correlations in relevant traits. In spite of considerable change in body size and brain size, no significant change in their covariation occurred either between the selection lines or between sexes. The relevance of these results to a brain and body size ‘scaling effect’ during evolutionary divergence is discussed.

Olfactomedin-related proteins are secreted glycoproteins with conserved C-terminal motifs. Olfactomedin was originally identified as the major component of the mucus layer that surrounds the chemosensory dendrites of olfactory neurons. Homologues were subsequently found also in other tissues, including the brain and in species ranging from Caenorhabditis elegans to Homo sapiens. Most importantly, the TIGR/myocilin protein, expressed in the eye and associated with the pathogenesis of glaucoma, is an olfactomedin-related protein. The prevalence of olfactomedin-related proteins among species and their identification in different tissues prompted us to investigate whether a gene family exists within a species, specifically Homo sapiens. A GenBank search indeed revealed an entire human gene family of olfactomedin-related proteins with at least five members, designated hOlfA through hOlfD and the TIGR/myocilin protein. hOlfA corresponds to the rat neuronal AMZ protein. Phylogenetic analyses of 18 olfactomedin-related sequences resolved four distinct subfamilies. Among the human proteins, hOlfA and hOlfC, both expressed in brain, are most closely related. Northern blot analyses of 16 human tissues demonstrated highly specific expression patterns: hOlfA is expressed in brain, hOlfB in pancreas and prostate, hOlfC in cerebellum, hOlfD in colon, small intestine and prostate and TIGR/myocilin in heart and skeletal muscle. The link between TIGR/myocilin and ocular hypertension and the expression of several of these proteins in mucus-lined tissues suggest that they play an important role in regulating physical properties of the extracellular environment. Future studies can now assess whether other members of this gene family, like TIGR/myocilin, are also associated with human disease processes.